Long non-coding RNA MALAT1 interaction with miR-429 regulates the proliferation and EMT of lung adenocarcinoma cells through RhoA.

Homo sapiens metastasis associated lung adenocarcinoma transcript 1 (LncRNA MALAT1) plays an important role in many types of cancer, but its role in human lung adenocarcinoma (LAC) is still unclear. In this paper, we found that LncRNA MALAT1 had high expression in human LAC tissues (vs. paracancerous normal tissue) and human lung adenocarcinoma cells (vs. human normal lung tissue cells). The expression of lncRNA MALAT1 was significantly associated with human lung adenocarcinoma tumor size, lymph node metastasis, and TNM staging, and was negatively correlated with miR-429 expression in lung adenocarcinoma tissues. In vitro, LncRNA MALAT1 could block human LAC cells in the G1 phase to inhibit proliferation by reducing the expression of cyclin D1 protein. LncRNA MALAT1 could inhibit the invasion and migration of human LAC cells by decreasing the expression of MMP-9 and vimentin and increasing the expression of E-cadherin. We also found that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-429 and directly suppressed the expression of RhoA protein. RhoA knockout and transfection of miR-429-mimic could play the same function which is to decrease the expression of cyclin D1, MMP-9, and vimentin proteins and increased E-cadherin protein expression. These results suggested that LncRNA Malat1 could promote the proliferation and EMT of human lung adenocarcinoma cells by competing with RhoA for binding to miR-429. IJCEP